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Linda D. Siracusa
Thomas Jefferson University
86Publications
34H-index
4,788Citations
Publications 82
Newest
#1Felicia Cooper (Thomas Jefferson University)H-Index: 1
#2Andrew M. Overmiller (Thomas Jefferson University)H-Index: 3
Last.Mỹ G. Mahoney (Thomas Jefferson University)H-Index: 12
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In addition to playing a role in adhesion, desmoglein 2 (Dsg2) is an important regulator of growth and survival signaling pathways, cell proliferation, migration and invasion, and oncogenesis. Although low-level Dsg2 expression is observed in basal keratinocytes and is downregulated in nonhealing venous ulcers, overexpression has been observed in both melanomas and nonmelanoma malignancies. Here, we show that transgenic mice overexpressing Dsg2 in basal keratinocytes primed the activation of mit...
1 CitationsSource
#2F. Cooper (PSU: Pennsylvania State University)
Last.My G. MahoneyH-Index: 14
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#1Karen M. Bussard (Thomas Jefferson University)H-Index: 12
#2Linda D. Siracusa (Thomas Jefferson University)H-Index: 34
Alterations in mitochondrial DNA (mtDNA) were once thought to be predominantly innocuous to cell growth. Recent evidence suggests that mtDNA undergo naturally occurring alterations, including mutations and polymorphisms, which profoundly affect the cells in which they appear and contribute to a variety of diseases, including cardiovascular disease, diabetes, and cancer. Furthermore, interplay between mtDNA and nuclear DNA has been found in cancer cells, necessitating consideration of these compl...
9 CitationsSource
#1Linda D. Siracusa (Thomas Jefferson University)H-Index: 34
#2Karen M. Bussard (Thomas Jefferson University)H-Index: 12
Metastases cause more than 90% of the morbidity and mortality associated with human cancers. Gene expression signatures associated with cancer progression and metastasis serve as unique tools to assist in patient diagnosis, prognosis, and treatment. Various types of signatures have been identified, ranging from those that are tumor-intrinsic or specific to a particular cancer subtype [1] to genes associated with a specific clinical outcome (e.g., “poor prognosis gene signature”) [2], as well as ...
Source
#1Stephanie C. Nnadi (Thomas Jefferson University)H-Index: 3
#2Xiang Wang (Thomas Jefferson University)
Last.Linda D. Siracusa (Thomas Jefferson University)H-Index: 34
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The adenomatous polyposis coli (APC) tumor suppressor gene is mutated in Familial Adenomatous Polyposis (FAP), an inherited disorder that predisposes individuals to developing intestinal polyposis and eventually leads to cancer. In the Min mouse model, the genetic background of mice carrying a mutation in the murine homolog of the APC gene (ApcMin) is critical to the manifestation of tumor phenotypes, as inbred strains have been demonstrated to differ dramatically in their susceptibility to poly...
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#1Jayanthi ManneH-Index: 4
#2Marina MarkovaH-Index: 4
Last.Sergio A. Jimenez (Thomas Jefferson University)H-Index: 69
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The Tight Skin mouse is a genetically induced animal model of tissue fibrosis caused by a large in-frame mutation in the gene encoding fibrillin-1 (Fbn-1). We examined the influence of gender on the collagen content of tissues in C57BL/6J wild type (+/+) and mutant Tight Skin (Tsk/+) mice employing hydroxyproline assays. Tissue sections were stained with Masson's trichrome to identify collagen in situ. Adult Tsk/+ mice skin contains ~15% more collagen, on average, than skin from +/+ mice of the ...
8 CitationsSource
#1Stephanie C. NnadiH-Index: 3
#2Rayneisha WatsonH-Index: 1
Last.Linda D. SiracusaH-Index: 34
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Every year thousands of people in the USA are diagnosed with small intestine and colorectal cancers (CRC). Although environmental factors affect disease etiology, uncovering underlying genetic factors is imperative for risk assessment and developing preventative therapies. Familial adenomatous polyposis is a heritable genetic disorder in which individuals carry germ-line mutations in the adenomatous polyposis coli (APC) gene that predisposes them to CRC. The Apc Min mouse model carries a point m...
8 CitationsSource
#1Oksana B. Serebrennikova (Tufts University)H-Index: 4
#2Christos Tsatsanis (Tufts University)H-Index: 36
Last.Philip N. Tsichlis (Tufts University)H-Index: 70
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To address the role of Tpl2, a MAP3K8 that regulates innate/adaptive immunity and inflammation, in intestinal tumorigenesis, we crossed a Tpl2 KO allele into the Apcmin/+ genetic background. Here, we show that Apcmin/+/Tpl2−/− mice exhibit a fivefold increase in the number of intestinal adenomas. Bone marrow transplantation experiments revealed that the enhancement of polyposis was partially hematopoietic cell-driven. Consistent with this observation, Tpl2 ablation promoted intestinal inflammati...
38 CitationsSource
#1Rayneisha WatsonH-Index: 1
#2Julie InnocentH-Index: 1
Last.Linda D. SiracusaH-Index: 34
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#1Monica J. Justice (BCM: Baylor College of Medicine)H-Index: 38
#2Linda D. SiracusaH-Index: 34
Last.A. FrancisstewartH-Index: 59
view all 3 authors...
The mouse is the leading organism for disease research. A rich resource of genetic variation occurs naturally in inbred and special strains owing to spontaneous mutations. However, one can also obtain desired gene mutations by using the following processes: targeted mutations that eliminate function in the whole organism or in a specific tissue; forward genetic screens using chemicals or transposons; or the introduction of exogenous transgenes as DNAs, bacterial artificial chromosomes (BACs) or ...
38 CitationsSource
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